The relative mobility of many organs of the human body is a prerequisite of optimal function. In this respect, it is important that such organs are able to move and slide in relation to adjacent organs and/or in relation to the body cavities within which they are enclosed. For example, if the oesophagus, the stomach, the intestines, the liver and the urogenital organs were not at least partially mobile in relation to adjacent organs and the abdominal wall and the diaphragm, functional disturbances would occur, such as the restriction of respiratory movement, hampered movement of intra-abdominal structures, intestinal obstruction and/or infertility.
If an organ receives a physical trauma, such as an injury, surgery, a burn or an electric shock, or experiences inflammation as a result of a pathogenic cause, one of the inevitable consequences of the healing and inflammatory processes which follow is the formation of adhesions and scar tissue, which may naturally restrict the aforementioned organ mobility.
Adhesions and scar tissue are formed as a result of the formation of a fibrin-platelet network following physical trauma or pathogenic inflammation, and the subsequent rebuilding and replacement of this network by granulation tissue.
The complex and typically highly irregular structure of the fibrin-platelet network, formed at an early stage after the trauma or as a result of inflammation, is of key importance in the fate of any wound healing process. Any physical structure, particularly filaments and membranes, whether diffusely or distinctly outlined, acts as a guide for the invading granulation tissue. This newly formed tissue is, in accordance with the mechanism described above, eventually rebuilt as scar tissue, organised as fibrous strands or membranes. The invading granulation tissue cells can practically never fully substitute for the original cells and, as a result, the tissue is never regenerated, but merely repaired. This is true for both the skin and for mucosal membranes, including those lining the body cavities, as well as other structures including muscles, tendons and nerves. Moreover, the scar tissue so formed may, in time, contract and remain contracted, deforming and disorganising the injured area.
The proliferation and invasion of fibrin threads by even a few granulation tissue cells (including angiogenic cells) is usually sufficient to induce the formation of adhesions. The direction, density and organization of the individual fibrin threads in the fibrin-platelet network of the clot provides information, and determines the track to be taken by the invading granulation tissue cells, as well as by specific cells such as Schwann cells. Extracellular fibrin may deposit, stick to and establish abnormal bridges between adjacent structures.
Thus, the structure of the fibrin-platelet network is of key importance in guiding the invading granulation tissue and thus in the formation of adhesions and scar tissue.